Complement regulatory proteins (CD46, 55 and 59) expressed on Schwann cells: immune targets in demyelinating neuropathies?

Miyaji K 1 , Paul F 2 , Shahrizaila N 3 , Umapathi T 4 , Yuki N 5

Affiliations 

  • 1 Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
  • 2 NeuroCure Clinical Research Center, Charité University Medicine, Berlin, Germany; Clinical and Experimental Multiple Sclerosis Research Center, Department of Neurology, Charité University Medicine, Berlin, Germany
  • 3 Division of Neurology, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
  • 4 Department of Neurology, National Neuroscience Institute, Singapore
  • 5 Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. Electronic address: mdcyuki@nus.edu.sg
J Neuroimmunol, 2014 Nov 15;276(1-2):172-4.
PMID: 25156074 DOI: 10.1016/j.jneuroim.2014.08.004

Abstract

Given their localization and important role in regulating complement, complement regulatory proteins may act as target antigens and their antibodies as biomarkers in demyelinating neuropathies. We investigated the binding of autoantibodies to complement regulatory proteins (CD46, 55 and 59) in demyelinating diseases. In 42 acute inflammatory demyelinating polyneuropathy, 23 chronic inflammatory demyelinating polyneuropathy, 13 acute motor axonal neuropathy, 71 multiple sclerosis, and 19 neuromyelitis optica patients as well as 55 healthy controls, we were unable to detect significant titers of antibodies to CD46, CD55 and CD59. These autoantibodies are unlikely to be biomarkers in acute and chronic inflammatory demyelinating polyneuropathies.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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